PMN recruitment and sequestration to sites of inflammation and second organ injury is initiated by pro-inflammatory mediators, among which LTB.sub.4 is considered to be very important (Weissmann, G., Smolen, J. E., and Korchak, H. M. 1980. Release of inflammatory mediators from stimulated neutrophils. N. Engl. J. Med. 303: 27-34; Sammuelsson, B. 1983. Leukotrienes: Mediators of inflammation and immediate hypersensitivity. Science 220: 568-575). Recently, the LTB.sub.4 receptor (BLTR) was also shown to serve as a coreceptor for HIV-1 entry, which further emphasizes the crucial role of this system in host defense (Owman, C. 1998. The leukotriene B.sub.4 receptor functions as a novel type of coreceptor mediating entry of primary HIV-1 isolates into CD4-positive cells. Proc. Natl. Acad. Sci. USA 95: 9530-9534). Aspirin is widely used for its anti-inflammatory and analgesic properties with several newly identified therapeutic actions including prevention of cardiovascular diseases and decreasing incidence of lung, colon and breast cancers, which increases the importance of obtaining complete knowledge of aspirin's mechanism of action (Marcus, A. J. 1995. Aspirin as prophylaxis against colorectal cancer. N. Eng. J. Med. 333: 656-658). When aspirin is given, in addition to inhibiting prostanoid biosynthesis, it also triggers the endogenous transcellular production of 15 epimeric or 15R LXA.sub.4, termed aspirin-triggered LXA.sub.4 (ATL), which appears to mediate in part some of aspirin's therapeutic impact and is generated in vivo (Serhan, C. N. 1997. Lipoxins and novel aspirin-triggered 15-epi-lipoxins (ATL). Prostaglandins 53: 107-137; Chiang, N., Takano, T., Clish, C. B., Petasis, N. A. and Serhan C. N. 1998. Aspirin-triggered 15-epi-Lipoxin A.sub.4 (ATL) generation by human leukocytes and murine peritonitis exudates: development of a specific 15-epi-LXA.sub.4 ELISA. J. Phar. Exp. Ther. 287: 779-790). LXA.sub.4 controls leukocyte responses via its own specific G protein coupled receptor, denoted ALXR, which also engages 15-epi-LXA.sub.4 (Serhan, C. N. 1997. Lipoxins and novel aspirin-triggered 15-epi-lipoxins (ATL). Prostaglandins 53: 107-137; Takano, T., Clish, C. B., Gronert, K., Petasis, N. A. and Serhan C. N. 1997. Neutrophil-mediated changes in vascular permeability are inhibited by topical application of aspirin-triggered 15-epi-lipoxin A.sub.4, and novel lipoxin B.sub.4 stable analogues. J. Clin. Invest. 101: 819-826). Like other local mediators, LXs are rapidly generated, evoke responses and are inactivated by further metabolism (Serhan, C. N. 1997. Lipoxins and novel aspirin-triggered 15-epilipoxins (ATL). Prostaglandins 53: 10714 137). Methods to monitor, study and screen potential pharmaceuticals, e.g., antiinflammatories, which interact with the identified receptors, therefore, are of interest.